Romano M F, Valerio G, Turco M C, Spadaro G, Venuta S, Formisano S
Dipartimento di Biologia e Patologia Cellulare e Molecolare, II Facoltà di Medicina e Chirurgia, Napoli, Italy.
Cell Immunol. 1992 Jan;139(1):91-7. doi: 10.1016/0008-8749(92)90102-u.
In the present work we analyzed the proliferative response of T lymphocytes from 11 atopic patients stimulated in vitro via either the CD2 or the CD3 pathway of cell activation. In both cases we found a significant decrease of thymidine incorporation in cell DNA in comparison with T cells from normal donors. The mechanism of this impaired proliferative response was analyzed. Atopic patients' T cells were found to secrete low quantities of interleukin 2 (IL2) and to express low amounts of Tac antigen, measured as both a percentage of Tac-positive cells and a mean fluorescence intensity of Tac antigen per cell. Addition of recombinant IL2 to cultures completely restored both cell proliferative response and Tac antigen expression. This effect was specific of IL2 since addition of IL1 or IL4 did not significantly affect T cell proliferative response. We conclude that atopic patients' T lymphocytes have a defect in both CD2 and CD3 pathways of cell activation relying on impairment of IL2 production, without involving IL2 responsiveness or other lymphokine defects.
在本研究中，我们分析了11名特应性患者的T淋巴细胞经细胞活化的CD2或CD3途径体外刺激后的增殖反应。在这两种情况下，我们发现与正常供体的T细胞相比，细胞DNA中胸苷掺入量显著降低。我们分析了这种增殖反应受损的机制。发现特应性患者的T细胞分泌少量白细胞介素2（IL2），并且Tac抗原表达量低，这是以Tac阳性细胞百分比和每个细胞Tac抗原的平均荧光强度来衡量的。向培养物中添加重组IL2可完全恢复细胞增殖反应和Tac抗原表达。这种作用是IL2特有的，因为添加IL1或IL4对T细胞增殖反应没有显著影响。我们得出结论，特应性患者的T淋巴细胞在细胞活化的CD2和CD3途径中均存在缺陷，这依赖于IL2产生受损，而不涉及IL2反应性或其他淋巴因子缺陷。
